Die Bedeutung des p75-Neurotrophinrezeptors während der De- und Remyelinisierung im Cuprizon- Modell der Multiplen Sklerose

Schüle, Susann-Cathrin

dc.contributor.advisor	Stadelmann-Nessler, Christine Prof. Dr.	de
dc.contributor.author	Schüle, Susann-Cathrin	de
dc.date.accessioned	2013-05-30T09:41:36Z	de
dc.date.available	2013-06-18T22:50:06Z	de
dc.date.issued	2013-05-30	de
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-001D-AF1C-3	de
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-3851
dc.language.iso	deu	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.ddc	610	de
dc.title	Die Bedeutung des p75-Neurotrophinrezeptors während der De- und Remyelinisierung im Cuprizon- Modell der Multiplen Sklerose	de
dc.type	doctoralThesis	de
dc.title.translated	The significance of the p75NTR during de- and remyelination in cuprizone-induced demyelination of Multiple Sclerosis	de
dc.contributor.referee	Zerr, Inga Prof. Dr.	de
dc.date.examination	2013-06-11	de
dc.description.abstracteng	Multiple sclerosis (MS), the most frequent central nervous system (CNS) autoimmune disease is characterized by multiple focal demyelinated lesions. Partial remyelination of these lesions is frequently observed and considered to be one of the factors contributing to the remission of symptoms. Neurotrophins are cytokines, which occur not only in the CNS and in the peripheral nervous system (PNS) but also in the immune system. Their effects are mediated through two different kinds of receptors, the tropomyosin- related kinase receptor (trk) and the p75 neurotrophin receptor (p75NTR), which can trigger different or even opposing effects. They can either promote apoptosis and pro-inflammatory pathways or support axonal regeneration. With regard to remyelination, it is well known that p75NTR is able to foster regenerative procedures in the PNS, whereas its role in the CNS has still to be clarified. This thesis examines the effects of p75NTR deficiency focussing on the extent of de- and remyelination, axonal damage and immigration of CD3+-T-cells into the CNS. To induce cerebral demyelination in wildtype- and p75NTR -deficient mice, the animals were exposed to cuprizone diet. The extent of remyelination was evaluated after stopping the cuprizone diet. At the time point of demyelination, no differences between wildtype- and p75NTR deficient mice were found regarding the extent of demyelination, axonal damage and number of infiltrating CD3+-T-cells. However, studying the time point of remyelination, the amount of axonal damage was significantly higher and also a tendency towards reduced remyelination and elevated number of immigrated CD3+-T-cells was observed in the absence of p75NTR expression. Thus, this work suggests that the expression of p75NTR might be helpful for regeneration not only the in the PNS but also in the CNS.	de
dc.contributor.coReferee	Oppermann, Martin Prof. Dr.	de
dc.subject.ger	p75-Neurotrophinrezeptor	de
dc.subject.ger	Remyelinisierung im Cuprizon- Modell	de
dc.subject.eng	p75NTR	de
dc.subject.eng	Multiple Sclerosis	de
dc.subject.eng	Remyelination	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-001D-AF1C-3-9	de
dc.affiliation.institute	Medizinische Fakultät	de
dc.subject.gokfull	Medizin (PPN619874732)	de
dc.description.embargoed	2013-06-18	de
dc.identifier.ppn	747316619	de

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